Increases in Genetic Information

Why would that be the only evidence? On another thread, you argue that you can infer the intelligent design of a creator god by indirect evidence, rather than by directly observing him creating, for example, complex multicellular eukaryotes. So, why would it be necessary to directly observe demonstrably real processes like mutation, selection and drift adding "new never before existed information", as you put it, to the genomes of multicellular eukaryotes? Surely we can indirectly observe the results of established processes if, according to you, we can indirectly observe the results of an unestablished process, like a god creating something. What would "new never before existing information" arriving in a multicellular organism look like? Are you suggesting that bacteria are designed to accumulate new information, and multicellular eukaryotes aren't? What about single celled eukaryotes? Have you observed a god designing bacteria? If not, why is there "good reason" to think that they were so designed? Indirect evidence? Can we look at the genomes of multicellular organisms in the present and find evidence of past events on them? If not, why not? Edited by bluegenes, : No reason given.

So, any mutation that makes a change in the phenotype of an organism would satisfy your demands. If you can observe variation within species, and if you can establish that species can change over time, then you have a reason to believe that common descent is "possible". Here's another fact. Intelligent designers exist, and they do so by "use of high amounts of incredibly specified information". So, it would be irrational to conclude that "high amounts of incredibly specified information" require intelligent design, wouldn't it? Specified information, therefore, does not require intelligent design, but intelligent designers do require specified information according to the observations we can make. Why haven't you observed that all known intelligent beings form from DNA? Are you incapable of observing this? So, since we have observed novel specified information forming by unintelligent processes like reproduction with variation, and since we have observed that specified information is a prerequisite for all known intelligent designers, the "scale of logic" makes "the I.D. theory" look like a non-starter. You mean one mutation that causes a specific change in the phenotype of one organism? We have observed many, which might help explain to you why biologists are evolutionists, and hillbillies are intelligent designists. Presumably, then, we would have to observe a non-living intelligent designer adding "never before existed information" to the chromosomal DNA of a multi-celled organism, or creating one from scratch, in order to advocate I.D. as an explanation of the origin of species and of life. If those are your standards, stick to them. Are you talking about the genetic code or similarities in the genomes of different species? If the latter, why give the penguins and ratites so much bird genetic material, and why give fully aquatic mammals lung genes instead of gill genes, and why make fossils that have both reptile and mammal features as well as fossils with both fish and amphibian features? To make it look as though evolution happens big time?Anyway, on "information" increase. Functional duplications of genetic material can be observed on eukaryote genomes, so the evidence that they can increase in information content is excellent.

You must be one of the few I.D. advocates who has never heard of bacterial flagella. Also, apparently, one of the few who doesn't seem to know that the many highly imobile plants you see all around you are multi-cellular. You could just give them all motility by designing a flagellum for the non-motile ones. That's true of the non-motile ones, certainly. Why does the advantageous characteristic of being able to react to environmental conditions indicate intelligent design to you rather than natural selection (design by unintelligent environments). I don't mean just the specific adaption being selected for, but also the capacity to adapt, which is advantageous.Your own cells show plasticity in relation to the environment when you tan in the sun, a process that protects their DNA from damage.What is your point, here? Are you suggesting that the nylon-eating bacteria can gain a novel function without novel "specified information"? And are you sure that you want to keep bringing up plasmids, which could be regarded as a very good example of a source of unintelligent non-living specified information?As you expressed an interest in novel specified information in multi-cellular eukaryotes in your other reply to me, here's an example for you. It explains the formation of a new coding gene in fruit flies. New gene, new protein

Duplications of sections of the genome are a common form of mutation. They can contain one or more coding genes, and biologists can identify the resulting paralogs on genomes.Here's a ten year old review which explains the process quite well, and includes sections on subfunctionalization and neofunctionalization, both important ways of adding new functional genes, which is what you're asking about in the O.P. Evolution by gene duplication: an updateIn your O.P., you quote this from a source:

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The average human has about "3164.7 million chemical nucleotide bases"

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The reason it says "average human" is because we vary in genome size. Different individuals have different duplications and deletions. So, genome size can vary within species. Therefore genomes can grow or diminish in size over time by both natural selection and drift (neutral evolution), which partially explains one of the things you're asking about in the O.P. (getting from a small relatively simple genome to some of the large complicated modern ones). The review I linked to explains an example in the Douc langur monkey, and beneficial duplications have been observed directly in labs.

That doesn't contradict what I said, does it? And mutations are known to cause new variants. Unless you can find a mechanism that stops species changing over time, you have to agree that common descent is "possible". Information enters population groups from the environment. The environments aren't intelligent, yet they are a source of information. Duplications of genetic material give the environments more material to work on. That's one way to get increases in genetic information.Here's an example: NeofunctionalizationHere's a ten year old review of what was known about duplication at the time (it predates much of the research on it, like the fish paper above). Evolution by gene duplication: an updateIf you understand these papers and others like them, you can see that there's excellent evidence for past increases in genetic information by mutation, selection and drift. Are you disagreeing with the observation that "specified information", by your own definition, is a prerequisite for all known intelligent designers? If you can't find an exception, why are you theorizing that intelligent design is the origin of all specified information? The production of new unique individual sexually reproducing eukaryotes with unique genomes carrying their own batch of new mutations isn't pre-programmed. No-one designed your unique genome, which combines old information in a unique way to make new information, as well as having its novel set of new mutations. You are specified by that unique genome in combination with the unique particular environment in which you developed. You and I are novelties requiring specific information. Again, do you mean the genetic code, or new added coding genes? If the latter, duplications of coding genes have been observed on the genomes of all organisms studied so far. And paralogs with different functions are readily observed as well, as you can see from the papers I've linked to.Edited by bluegenes, : Added last sentence

I did. Mutations are what creates novel variation. I said: Yes, they do. You said: Which didn't contradict what I was saying about common descent, and is also badly worded. Neither natural selection nor drift create the variation. They are the processes that change the frequency of variants. Of course the variants are there before natural selection can act on them.Whenever a new mutation that effects the phenotype in a specific way occurs in an individual, that is novel "specified information".In the rest of the post you're replying to, I gave you some papers to read with examples of past increases in genetic information and increases in the quantity of protein coding genes occuring in eukaryotes. They show clear examples of what this thread is about. "Increases in genetic information".I hope you enjoyed the papers.

How do you expect something to be observed before it exists, and how do you expect natural selection to act on anything other than "already existing genes"?Mutations that have happened in the past can be observed on genomes. And that last bit is how information enters population groups from their environments. It's called the theory of natural selection. But it's not new, and I can't take credit for it. Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict.The paper answers your question. Geneticists know how to distinguish duplications from deletions. The original anti-freeze gene is on an insertion. Then there are multiple copies of it on tandem duplications. The sequence of mutations involved are traceable. The effects of past events can be observed in the present. When you go out of your house in the morning, and observe that the ground is soaking wet and the trees are dripping, you can figure out that it has rained during the night. Have you invented time travel in making an indirect observation of a past event? Is time travel necessary in order to convict a murderer on forensic evidence beyond all reasonable doubt? Is time travel necessary to infer a past river from a dried river bed?History can be observed on genomes. You can look at the genomes of two species and see that the differences which are at fixation between them are caused by exactly the same processes that cause the differences between different breeds of the same species and different individuals within a species. If you can get the big roarer cats (lions ,tiger, leopard, jaguar) from a common ancestral group, as the O.P. suggests, then you can get lions and domestic cats from a common ancestral group, and cats and dogs from a common ancestral group. There's nothing to stop the quantity of differences that separate them happening. If you think common descent is impossible, you need to tell us about this unknown mechanism of yours which limits the quantity of mutations that can go to fixation in diverging population groups. A novelty in one species isn't used to show its relationship to another species which lacks that novelty. We infer close common ancestry from similarities, not differences! And you've misunderstood the fish paper. Paralogs can be identified by looking within just one species. In the paper, they show the area in which the L. dearborni insertion has happened in G. aculeatus to show what the area was probably like before the event, but that is not how they know that a duplication has taken place. It is by the sequence identity of the duplicated section. Paralogs have been observed in the genomes of all species whose genomes have been examined, and duplications occur regularly in individual organisms. The researchers trace the mutational history of the formation of the AFPIII genes from LdSAS-B. You can if you know how to read history on genomes. That demand for direct observation would invalidate all hypotheses on the origin of species, and all science that deals with the past. How many non-biological intelligent beings have we directly observed making genes, life, or anything else? Alleles have to exist before they can be selected, and if by "loss of information" you mean loss of diversity, that is caused by bottlenecks and extinction events, not by speciation. That's not how they conclude it. The paper is actually about how it evolved. It did it by insertion, deletion, point mutations, and tandem duplications. All are common forms of mutation. There's no big mystery about "increases in genetic information", the subject of this thread. They do not require intelligent design, but all known intelligent designers do require them. But you do have your own mutations, and so did your parents have theirs, some of which you will have inherited. But even without those, your uniqueness, by definition, involves very specific information, yet no-one designed you, which was my point. Dollar bills don't duplicate themselves, but genes do. You can start out with a "simple single celled" organism, and watch it evolve into strains with duplications in less than one year, if you want to.

Your links contain mistakes and completely unsupported claims. On another thread, you ask how you can trust the information in peer reviewed papers, but you seem to have no problems accepting the validity of those two articles.Let's take the first one. Brian Thomas on fruit flies.

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If evolutionary biologists could document such evolution in action, they could vindicate their worldview and cite real research to support their surreal claims. In 1980, this search for proof led researchers to painstakingly and purposefully mutate each core gene involved in fruit fly development. The now classic work, for which the authors won the Nobel Prize in 1995, was published in Nature. The experiments proved that the mutation of any of these core developmental genes. Mutations that would be essential for the fruit fly to evolve into any other creature merely resulted in dead or deformed fruit flies. This therefore showed that fruit flies could not evolve.

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Here's the paper he's referring to: Nusslein-Volhard, C. and E. Wieschaus. 1980 Immediately, you can see from the authors' description of what they are doing that it is not what your article claims at all.From the paper:

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In systematic searches for embryonic lethal mutants of Drosophila melanogaster we have identified 15 loci which when mutated alter the segmental pattern of the larva. These loci probably represent the majority of such genes in Drosophila. The phenotypes of the mutant embryos indicate that the process of segmentation involves at least three levels of spatial organization: the entire egg as developmental unit, a repeat unit with the length of two segments, and the individual segment.

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What they are doing is trying to find the genes that are involved in the development of the segmental pattern of the flies, and also at what stage of the development particular genes are involved. The easiest way to do this is to damage genes or knock them out completely and see which ones effect the segmental pattern and at what stage of development is altered. It's common sense. What they do not do is try out all the possible mutations that could happen on the fifteen genes that they identify (or any other genes) to see if any are neutral or could be advantageous in certain circumstances. That's impossible to do because there are so many different ways in which the genes can mutate. So, there's nothing at all in that paper that shows that those fifteen genes or any other fruit fly genes can't change over time.Then your author goes on to make more mistakes about another paper. My comments in yellow.

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In a recent study, also published in Nature, University of California Irvine researcher Molly Burke led research into the genetic changes that occurred over the course of 600 fruit fly generations. The UCI lab had been breeding fruit flies since 1991, separating fast growers with short life spans from slow growers with longer life spans.5

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The UCI scientists compared the DNA sequences affecting fruit fly growth and longevity between the two groups. After the equivalent of 12,000 years of human evolution, the fruit flies showed surprisingly few differences.

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The group facing selection for rapid development went from egg to adult ~20% faster than their ancestors and the control group. In terms of any possible new mutations occuring and contributing to this, it would only be the equivalent of 12,000 years of human evolution if the population sizes were the same. About 10,000 fruit flies were involved in the experiment. If mutation rates are about the same, an effective human population size of 100,000 would mean 1,200 years. No one would expect much to happen in a population of 10,000 sexually reproducing eukaryotes in 600 generations excepting, ironically, those young earth creationists who argue for lots of rapid diversification since the Ark bottleneck!

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One requirement for Darwin's theory is that the mutational changes that supposedly fuel evolution somehow have to be "fixed" into the population. Otherwise, the DNA changes quickly drift right back out of the population. No, they don't.

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The researchers found no evidence that mutational changes relevant to longevity had been fixed into the fruit fly populations.

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The study's authors wrote, "In our sexual populations, adaptation is not associated with 'classic' sweeps whereby newly arising, unconditionally advantageous mutations become fixed."

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They suggested that perhaps there has not been enough time for the relevant mutations to have become fixed. They also suggested an alternativethat natural selection could be acting on already existing variations. But this is not evolution, and it is actually what creation studies have been demonstrating for many years.

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Evolution was not observed in fruit fly genetic manipulations in 1980, nor has it been observed in decades-long multigenerational studies of bacteria and fruit flies. The experiments only showed that these creatures have practical limits to the amount of genetic change they can tolerate. When those limits are breached, the creatures don't evolvethey just die.

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Although the experimental results from these studies were given titles with an evolutionary "spin," the actual experiments demonstrate undoubtedly that bacteria and fruit flies were created, not evolved.

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In the experiment, no actual new mutations that contributed to the specific characteristic being selected for were identified, although there could have been some. There could also have been mutations that were beneficial in other areas. However, that's not the important point. The selection that they observed in the lab could certainly have been on already existing variations.The wild population of any species of fruit fly will have far more than 600 times the number of individuals than there were in the experiment. In one generation (two weeks) more mutations will occur in that wild population than could occur in 600 generations in the lab. For that rather obvious reason, it's impossible for such experiments to demonstrate what cannot happen in the wild in terms of potentially advantageous mutations of any kind involving any characteristic.Why couldn't the author figure that out?I'll explain what's wrong with the other article on the Lenski experiment in my next post.

You see new information every time a mutation changes a phenotype.Why don't you just learn to read history on genomes? Here's the rest of the post you clicked on the reply button to, but avoided the point of:

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Mutations that have happened in the past can be observed on genomes.

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Just being real writes:

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bluegenes writes:

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Information enters population groups from the environment.

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Huh? Every bedtime story I’ve ever been told about evolution has the information building up by the process of random mutations (in the genetic code) and natural selection, selecting those traits which give the organism an advantage to survive over the others.

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And that last bit is how information enters population groups from their environments.

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JBR writes:

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I’ve never heard anyone claim that the environment actually puts the information in there. If you have some new scientific theory on this, I’d love to hear it.

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It's called the theory of natural selection. But it's not new, and I can't take credit for it.

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JBR writes:

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I have a question for you to consider when it comes to claiming that the antifreeze gene is an example of added new information to the DNA code. If two species in any order are compared, who determines which of the two species are the oldest and possesses the genes of the original configuration? This is important because once again, how do we know the antifreeze gene may not have been the original, and the others without the gene aren’t the result of loss of information?

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Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict.

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The paper answers your question. Geneticists know how to distinguish duplications from deletions. The original anti-freeze gene is on an insertion. Then there are multiple copies of it on tandem duplications. The sequence of mutations involved are traceable. The effects of past events can be observed in the present.

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Just being real writes:

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Did someone invent time travel and go back to take samples of the original?

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When you go out of your house in the morning, and observe that the ground is soaking wet and the trees are dripping, you can figure out that it has rained during the night. Have you invented time travel in making an indirect observation of a past event? Is time travel necessary in order to convict a murderer on forensic evidence beyond all reasonable doubt? Is time travel necessary to infer a past river from a dried river bed?

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History can be observed on genomes.

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Just being real writes:

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Rather it is bacteria, fossils, or fish, if you are trying to demonstrate A is related to Z there must be at least one observed path somewhere to show relationship is even possible.

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You can look at the genomes of two species and see that the differences which are at fixation between them are caused by exactly the same processes that cause the differences between different breeds of the same species and different individuals within a species. If you can get the big roarer cats (lions ,tiger, leopard, jaguar) from a common ancestral group, as the O.P. suggests, then you can get lions and domestic cats from a common ancestral group, and cats and dogs from a common ancestral group. There's nothing to stop the quantity of differences that separate them happening. If you think common descent is impossible, you need to tell us about this unknown mechanism of yours which limits the quantity of mutations that can go to fixation in diverging population groups.

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Just being real writes:

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You cannot use speculated relationship to prove added information, in order to prove relationship. If you do, now you are employing circular reasoning.

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A novelty in one species isn't used to show its relationship to another species which lacks that novelty. We infer close common ancestry from similarities, not differences! And you've misunderstood the fish paper. Paralogs can be identified by looking within just one species. In the paper, they show the area in which the L. dearborni insertion has happened in G. aculeatus to show what the area was probably like before the event, but that is not how they know that a duplication has taken place. It is by the sequence identity of the duplicated section. Paralogs have been observed in the genomes of all species whose genomes have been examined, and duplications occur regularly in individual organisms. The researchers trace the mutational history of the formation of the AFPIII genes from LdSAS-B.

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JBR writes:

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If you are trying to establish relationship with anything organic, you obviously can't observe this path over millions of years,.

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You can if you know how to read history on genomes.

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JBR writes:

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..so relationships between species are limited to what you can physically observe over relatively recent generations.

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That demand for direct observation would invalidate all hypotheses on the origin of species, and all science that deals with the past. How many non-biological intelligent beings have we directly observed making genes, life, or anything else?

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JBR writes:

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Yes, with speciation, we have observed small changes occur. But these changes can be (in most of the cases) shown to be the result of natural selection, selecting already existing alleles, and over time a loss of information.

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Alleles have to exist before they can be selected, and if by "loss of information" you mean loss of diversity, that is caused by bottlenecks and extinction events, not by speciation.

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JBR writes:

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The paper cited compares DNA of different species in order to conclude that fish have evolved an antifreeze protein.

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That's not how they conclude it. The paper is actually about how it evolved. It did it by insertion, deletion, point mutations, and tandem duplications. All are common forms of mutation. There's no big mystery about "increases in genetic information", the subject of this thread. They do not require intelligent design, but all known intelligent designers do require them.

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Just being real writes:

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bluegenes writes:

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No-one designed your unique genome

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My unique genome is a combination of pre-existing genes from my mother and my father. I did not receive some completely new information that did not exist which gave me spider man abilities or the ability to see infrared light.

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But you do have your own mutations, and so did your parents have theirs, some of which you will have inherited. But even without those, your uniqueness, by definition, involves very specific information, yet no-one designed you, which was my point.

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JBR writes:

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I thought jbozz21 did a good job of explaining what is meant, but allow me to try to simplify what I am talking about here. Imagine asking Donald Trump how he got so wealthy. If he said, Well I started out as a wee lad with only five dollars to my name, and I opened a bank account in one bank and then I transferred all the money across town to another bank and then to another, and kept doing this, occasionally losing a penny here and a penny there, but over time I amassed my great wealth. You would scratch your head in confusion because obviously you know that a person cannot get wealthy just moving the same money back and forth. Somewhere along the way a good deal of new funds has to be added to Mr. Trumps account in order for him to be so rich. Likewise you can’t start out with a simple single celled organism and claim that through millions of years of transferring the same gene pool of information back and forth, it can eventually evolve into an astrophysicist. Somewhere along the way we would have to introduce a whole lot of new genes that produce a whole lot of new and advanced phenotypes.

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Dollar bills don't duplicate themselves, but genes do. You can start out with a "simple single celled" organism, and watch it evolve into strains with duplications in less than one year, if you want to.

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If you disagree with the analysis of past mutations in this paper, tell us why. Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict.

On your second article:Bacteria 'evolving in the lab'? (Lenski, citrate-digesting E. coli) - creation.comThe article was written in 2008, and the author speculates on what happened in the Lenski experiment when one strain of E. coli evolved the ability to utilize citrate in oxic conditions. Here's a 2012 paper in which the researchers identify some of the mutations that contributed to the adaptation. So, you can see for yourself how wrong Don Batten's speculations are. A new regulatory gene was created by duplication and fusion after (probably) at least two potentiating neutral mutations, and then further mutations refined the system. There may well have been 7 or more mutations involved in some of the current cit+ organisms, and the process of refinement is "open ended" as the paper puts it (it is probably still going on).As one of the things you are asking about in the O.P. is increases in genetic material and increases in functional genetic material, the Lenski results with their multiple duplications are a good example of such increases happening in real time.Batten's also wrong and misleading on the development of chloroquine resistance in malarial parasites, but that's another very interesting subject.